Page 78 - JSOM Summer 2022

emergency intervention and are the result of decreased platelet If a patient has been treated with heparin, HIT may occur
production. Similarly, in 64% of thrombocytopenia patients, rapidly and sometimes within hours. In these instances, it is

platelet counts return to normal levels or remain stable. In the often life-threatening. HIT is characterized by the presence of
prehospital environment, dilution and drug-induced thrombo- platelet-activating antibodies, which can be identified through
cytopenia are the most common etiologies of thrombocytope- lab testing, that recognize the heparin–PF4 complexes in the

nia. The probability of developing immune thrombocytopenia blood. These antibodies then destroy the platelets. A key find-
has been estimated to be around 7%. 1 ing is whether the patient has just had a surgery, in addition
to a 50% decrease in platelet count from baseline. HIT affects
20–50% of patients and can affect the arterial and venous
Decreased Platelet Production
systems.
Suppression or dysfunction of the bone marrow, where plate-
lets are produced by megakaryocytes, can cause decreased Non–immune-mediated HIT can also occur during heparin
platelet production. Megakaryocyte production is regulated therapy. This type of HIT is caused by heparin and platelets
by a hormone produced by the kidneys and liver called throm- directly interacting in the blood; the effects are typically mild
bopoietin. A wide variety of medications can affect bone mar- with platelet counts quickly returning to normal levels. Other
row function. A complete history, including medication use, nonimmune causes of decreased platelet production are cer-
should be obtained on every patient when clinical conditions tain viral infections, dehydration, liver failure, sepsis, myelo-
allow. Medics should also be aware of possible myelosuppres- suppressive therapies (such as cancer treatments), congenital
sive effects of any routine medications being taken on deploy- predispositions, chronic alcohol use, vitamin B12 or folate
ment, such as proton pump inhibitors (PPIs) and isotretinoin (B9) deficiency, and bone marrow disorders. For example, in-
(Accutane). In cases in which the effects of medications are un- fection with leptospirosis can affect platelet production due to
known and there is a suspicion for medication-induced bone kidney failure or dysfunction and should be considered when
marrow dysfunction, subject matter experts or pharmacologi- suggested by the patient’s history.
cal resources should be consulted.
Immune thrombocytopenia (ITP) can result from several dif-
ferent mechanisms: 1) the suppression of megakaryocyte and
Splenic Sequestration
platelet development, 2) megakaryocyte apoptosis by ITP
Thrombocytopenia can also occur due to splenic dysfunction plasma/immunoglobulin G (IgG) or T cells, or 3) respon-
causing overaccumulation of platelets in the spleen after blood siveness to thrombopoietin receptor agonists (TRAs). Other
backs up and fails to circulate properly. This is also called con- pathogenic mechanisms beyond antibody-mediated apoptosis
gestive splenomegaly. When vasoconstriction occurs and the are antigen shedding and T-cell–mediated platelet destruction.
spleen cannot properly filter the blood in the body, congestive
splenomegaly prevents the aggregation of platelets needed for Additionally, there are disorders that cause decreased platelet
clotting. This dysfunction occurs when the spleen no longer survival such as alloimmune thrombocytopenia, disseminated
protects the body against infection, causing an overaccumula- intravascular coagulation (DIC), thrombotic thrombocytope-
tion of damaged and decayed erythrocytes and platelets that nic purpura (TTP), hemolytic uremic syndrome (HUS), use of
are not effectively disposed of by macrophages. Infiltrative certain medications, and cardiopulmonary bypass surgery.
diseases of the spleen (such as leukemia, systemic mastocyto-
sis, lymphoma, and amyloidosis), liver cirrhosis, and portal DIC can be a severe and fatal comorbidity in thrombocytope-
hypertension can cause this type of splenic dysfunction. The nia and is characterized by small blood clots forming through-
identification of these specific conditions can assist the medic out the body and blocking smaller blood vessels. This is a case
or field provider by increasing the index of suspicion based on where, in the absence of active bleeding, treatment methods
a history of these types of pathological diseases. do not include the transfusion of platelets due to a consump-
tive coagulopathy, where any platelets that are transfused are
quickly consumed and rendered ineffective (and even worsen
Increased Platelet Consumption
the condition). Typical clinical presentations are acute severe
The liver produces heparin, an anticoagulant, which prevents illness, bleeding, acute kidney failure, hepatic and respiratory
excessive fibrin formation during an inflammatory reaction. dysfunction, and hemodynamic collapse. DIC often follows
Unfractionated heparin and low molecular weight heparin are sepsis, trauma, or severe burns. If left untreated, DIC can eas-
medications that can be administered as an injection in order ily be fatal.
to prevent blood clots during surgery or periods of immobili-
zation, such as extended hospitalizations. Excessive amounts
of heparin can cause a patient to experience thrombocytope- Dilution
nia. Heparin forms a complex with a blood factor released by Dilutional thrombocytopenia is a temporary type of throm-
platelets, known as platelet factor 4 (PF4), that the immune bocytopenia that occurs after a patient receives a massive
system views as a foreign substance. The body then forms an transfusion that is typically over 15 units of PRBCs. A transfu-
antibody against the heparin–PF4 complex. sion of this magnitude, usually exceeding total blood volume
within 24 hours, is not uncommon in hemorrhagic emergen-
As a result of this process, patients that are treated with cies. Platelet dilution occurs when RBCs and crystalloids re-
hepa rin are at risk of heparin-induced thrombocytopenia place or dilute critical platelets. The platelet count will usually
(HIT). HIT occurs when a patient experiences an adverse im- return to normal once the patient’s circulatory system recovers
mune-mediated reaction to the drug and these patients are at or platelets are also transfused. This type of thrombocytope-
risk for venous or arterial thrombosis. Platelet counts can de- nia has become less common because platelet transfusions are
cline within 5–10 days with no previous exposure to heparin. administered before the platelet count can reach this critical

76 | JSOM Volume 22, Edition 2 / Summer 2022